Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Benzalkonium Compounds”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 289 records · Page 16Linked to original sources
PubMed1984

Noncovalent bonding of penicillin and cefazolin to dacron.

Dacron grafts treated with the surfactant, benzalkonium chloride or TDMAC bind significant quantities of penicillin-14C or cefazolin-14C. The treated grafts showed strong antibacterial activity which indicated that bound radioactivity corresponds to the reversible adsorption of biologically active molecules. Bound penicillin-14C or cefazolin-14C slowly dissociates when the grafts are placed in a surgically prepared muscle pouch in the rat. This slow release of antibiotic produces therapeutic levels of antibiotic in the adjacent tissue. Binding can also be achieved by in situ irrigation of surfactant treated grafts with antibiotic or by injection of the antibiotic.

Adsorption↗
PubMed1992

Inhibition and activation of porcine squalene epoxidase.

Pig liver squalene epoxidase (SE) has been partially purified from solubilized microsomes by DEAE-Sephacel and Blue Sepharose 4B chromatography. This stable and reproducible preparation was used to investigate the mechanism of several substrate-like inhibitors of SE and to study the effects of pH, metals, detergents, and cofactors on enzyme activity. Most divalent (1 mM) and trivalent (0.1 mM) metal cations had little effect on SE at pH 7.4; only ferrous and cupric ions showed ca. 50% reduction in SE activity. Interestingly, at pH 8.8, EDTA (10 mM) shows 1.8-fold enhancement of enzyme activity. Among the detergents, Triton X-100 was clearly superior for solubilization and purification of porcine SE; Tween 80, Lubrol-PX, 3-[(3-cholamidopropyl)dimethylammonio]propanesulfonic acid, octyl beta-glucoside, and three different Zwittergents were much less effective for SE solubilization. Partially purified pig liver SE showed maximal activity at pH 8.8-9.0. Trisnorsqualene alcohol and trisnorsqualene cyclopropylamine were noncompetitive inhibitors at pH 8.8, with Ki values of 4 microM and 180 nM, respectively; these two inhibitors were not substrates for SE. In contrast, 26-hydroxysqualene was both a competitive inhibitor with a Ki value of 4 microM at pH 8.8 and a substrate for SE. An unexpected enhancement (up to 350%) of SE activity was observed at pH 7.4 following preincubation with selected nonpolar derivatives of farnesol and farnesoic acid. At pH 8.8, this effect was less dramatic but still evident.

Animals↗
PubMed1983

Dermal glycosaminoglycans characterise the primary irritant dermatitis in psoriatics and healthy individuals.

Primary irritant dermatitis includes an inflammatory process of connective tissue which is of general interest. For the first time this process has been characterised biochemically in humans by following the dermal changes in the concentration of hydroxyproline and four glycosaminoglycans. In healthy individuals (n = 7) and in psoriatics (n = 8) the changes were rather similar. Only dermatan sulphate showed a tendency towards an abnormal response in the psoriatics. In both groups the deviations from the pre-irritant condition clearly distinguished the response of irritant dermatitis from that of the wound healing process: (1) the concentration of hyaluronic acid decreased by the third day and remained so until by the sixth day, (2) after a decrease on the third day the concentration of dermatan sulphate returned to the initial value by the sixth day, (3 and 4) the concentration of chondroitin 4/6-sulphate and heparan sulphate increased continuously from the third to the sixth day, and (5) the concentration of hydroxyproline remained constant throughout the period of investigation.

Adult↗
PubMed1986

Use effectiveness of a spermicidal suppository containing benzalkonium chloride.

A multicentric trial in 9 Spanish Clinics of Family Planning was conducted to evaluate the effectiveness of a vaginal contraceptive Ovule (suppository), containing 18.9 mg of benzalkonium chloride. Gynaecological and cytobacteriological examinations were made to evaluate any possible side-effect. Six-hundred-fifty-three women at risk of unwanted pregnancy accepted the method as the only contraception during 9,517 months. The results are expressed in life-tables (Tietze-Lewit). Net cumulative first segment rate at 12 months were: terminations 27.2; pregnancy 3.7; medical reason 2.3; planned pregnancy 2.8; other personal reasons 18.4. At 24 months the rates were: terminations 34.1; pregnancy 3.7; medical reason 2.6; planned pregnancy 6.5; personal reasons 21.3. Error or failure to use the spermicide resulted in 12 of 23 pregnancies (52%), while in another 4 pregnancies (17%) there were reasonable elements of doubt concerning its correct use. There were no gynaecological or cytological changes. We conclude that this product is a safe and very effective contraceptive if used according to the prescribed instructions and before any sexual encounter.

Adult↗
PubMed1991

Spermicide permeation through biocompatible polymers.

Although spermicides are safe and effective contraceptive/prophylactic agents, they are inconvenient to use. Formulations that provide a controlled release of spermicide may improve user acceptance, and therefore effectiveness. Using a two-chamber diffusion cell, we measured the rates of permeation of nonoxynol-9 (N9), benzalkonium chloride (BC), and chlorhexidine (CH) through films of ethylene-vinyl acetate copolymer (EVAc) and silicone elastomer (SILASTIC). In addition, we encapsulated N9, BC, and CH into solid polymer matrices and measured the rate of spermicide release following immersion in water. We also developed equations for predicting the release rate of spermicide from a vaginal ring containing encapsulated spermicide, and tested these equations using hollow SILASTIC rings containing pure N9 or BC. N9 diffuses through a thin film of SILASTIC several orders of magnitude slower than through water. The rates of permeation of N9 through EVAc, BC through SILASTIC, and CH through SILASTIC were too low to detect over a one-week experiment. Polymer matrices of EVAc or SILASTIC released N9 at a controlled rate for several days. Based on these measurements, we predict that a vaginal ring containing an inner core of EVAc/N9 surrounded by a thin, permeable layer of SILASTIC will provide a controlled, constant release of N9 for over 30 days. Because of its low permeability in SILASTIC, BC is probably not a good spermicide for a long-acting vaginal ring. Because of its low solubility in water, CH is also not a good candidate for controlled release into the vaginal mucus.

Benzalkonium Compounds↗
PubMed1993

Involvement of NK receptors and beta-adrenoceptors in nitric oxide-dependent relaxation of rabbit aorta rings following electrical-field stimulation.

Electrical-field stimulation caused an endothelium-dependent relaxation in rabbit aorta rings precontracted by phenylephrine. The relaxation was reduced in a dose-dependent manner by morphine, benzalkonium, [D-Pro2,D-Trp7,9]substance P and an beta-adrenoceptor antagonist, propranolol. The vasodilatation was enhanced by superoxide dismutase and abolished by haemoglobin and NG-monomethyl-L-arginine. The inhibitory effect of NG-monomethyl-L-arginine was reversed by L-arginine, the precursor of nitric oxide biosynthesis, but not by its enantiomer, D-arginine. These data show that the electrically induced relaxation is independent on nitric oxide released by NK receptors and beta-receptors. Moreover, morphine, by reducing substance P release, decreased the magnitude of electrically induced relaxation, suggesting an indirect role of opioids in the regulation of the peripheral circulation through the control of nitric oxide release. Furthermore our observations confirm the hypothesis that subtypes of beta-adrenoceptors releasing nitric oxide participate in the regulation of vascular tone.

Adrenergic beta-Antagonists↗
PubMed1995

Human and rat cutaneous mast cells: involvement of a G protein in the response to peptidergic stimuli.

Recent evidence suggests that peptides induce the release of mediators from rat peritoneal mast cell by means of a receptor-independent mechanism, possibly involving an interaction with sialic acid residues at the cell surface followed by the activation of a guanine nucleotide binding protein (G protein). We have now examined the potential involvement of sialic acid residues and of G protein stimulation in the activation of both human and rat cutaneous mast cells by neuropeptide Y, its C-terminal fragments and the wasp venom peptide, mastoparan. Neuropeptide Y-(18-36) was the most effective histamine releaser of the fragments tested, the order of potency being neuropeptide Y-(18-36) > neuropeptide Y-(22-36) > neuropeptide Y-(1-36). This order of potency suggests that the effects of the peptides are not mediated through classical NPY receptors. The hydrolysis of sialic acid residues by neuraminidase and the inhibition of G proteins by benzalkonium chloride or pertussis toxin significantly inhibited the secretory response of cutaneous mast cells to neuropeptide Y-(18-36) and mastoparan. These results demonstrate that the peptidergic pathway described for the activation of peritoneal rat mast cells is also involved in the response of cutaneous human and rat mast cells to peptides.

Animals↗
PubMed1989

The effect of epinephrine and benzalkonium chloride on cultured corneal endothelial and trabecular meshwork cells.

We evaluated the effect of dipivefrin hydrochloride, epinephrine hydrochloride, epinephrine borate and their respective vehicles with and without the preservative benzalkonium chloride, on the in vitro growth characteristics of human corneal keratocytes, endothelial cells and trabecular meshwork. Epinephrine hydrochloride and borate at low concentrations (0.0002%) significantly inhibited growth of both trabecular meshwork and corneal endothelial cells. Higher concentrations (0.02%) of these same drugs induced the same effect on the growth of keratocytes in vitro. Similar observations were made on the effect of dipivefrin hydrochloride on human corneal cells in vitro. Benzalkonium chloride alone was demonstrated to be responsible for the growth inhibitory effects on trabecular cells. The susceptibility of trabecular meshwork cells in culture to the commonly used ophthalmic preservative benzalkonium chloride is demonstrated.

Benzalkonium Compounds↗
PubMed1994

The scanning force microscopy of DNA in air and in n-propanol using new spreading agents.

We present recent advances in DNA specimen preparation technique for scanning force microscopy (SFM) based on spreading on mica in the presence of cationic and non-ionic detergents. Reproducible DNA imaging in air and in n-propanol has been achieved in the presence of the non-ionic detergent 2,4,6-tris(dimethylaminomethyl) phenol (DMP-30) or the cationic detergent cetylpyridinium chloride (CP) in a microdrop containing nanograms of DNA. In an alternative procedure, a microdrop of detergent is applied to the surface just prior to the DNA. Quantitative image analysis yields as the apparent molecular dimensions of the DNA a width of approximately 7 nm and a height of approximately 0.7 nm, and delineates the problems of DNA metrology by SFM.

1-Propanol↗
PubMed1987

Effect of chemical ablation of myenteric neurons on neurotransmitter levels in the rat jejunum.

We have quantified neurotransmitter changes in the rat jejunum in which the myenteric neurons were ablated by serosal application of benzalkonium chloride. Within 2 days after benzalkonium chloride treatment, there was a 40% reduction in the activity of choline acetyltransferase, a specific marker for cholinergic neurons, and a 25% reduction in the amount of vasoactive intestinal peptide per centimeter length of jejunum. By 15 days, levels were comparable to those in control segments, and by 45 days after myenteric neuronal ablation, levels in treated tissues were twice those in controls. In contrast, we observed no reduction in the amount of leucine-enkephalin per centimeter length of jejunum at early times after benzalkonium chloride treatment, although by 45 days, levels of this neurotransmitter in treated segments of jejunum were more than twice those in controls. Significant increases in muscle thickness and tissue weight were also observed at 15, 30, and 45 days after myenteric neuronal ablation. Thus we have observed that in response to chemical ablation of myenteric neurons in the rat jejunum, there is a thickening of the smooth muscle layers and a compensatory increase in the production of certain neurotransmitters by the surviving neuronal elements in the gut.

Animals↗
PubMed1991

Changes in the structure and regeneration mode of the rat small intestinal mucosa following benzalkonium chloride treatment.

Tritiated thymidine was administered IP to rats that had been exposed to benzalkonium chloride in the duodenum, jejunum, and ileum, resulting in neuronal ablation. Epithelial cell proliferation and migration were studied 21 and 7 days after treatment. Significant hyperplasia and hypertrophy of the villi and crypts was seen from day 7 on. This was half as pronounced as that of the muscle layer, whose maximal percent increase was not seen until day 21. In the crypt, the proliferation had increased significantly (65% 3H index corrected) and its zone had expanded proportionally to the total crypt depth. After an average of 36 hours in the ileum (48 hours in normal rats), labeled cells reached the tip of the lengthened villi, reflecting significantly accelerated migration. Concerning the distributional pattern of the labeled cells in the crypt, a nonsignificant shift to the lower two thirds of the crypt could be distinguished. From this the author concludes that treatment with benzalkonium chloride influences the proliferation and migration of the epithelial cells in the treated area. These alterations may result from loss of the myenteric plexus, but other factors cannot be excluded.

Animals↗
PubMed1993

Involvement of the myenteric plexus in the cholera toxin-induced net fluid secretion in the rat small intestine.

BACKGROUND: The enteric nervous system is responsible in vivo for most of the change in fluid transport induced by cholera toxin. The aim of the present study was to investigate the importance of the myenteric plexus in the Intramural reflex responsible for this secretion. METHODS: Long-term ablation of the myenteric plexus was achieved by serosal application of benzalkonium chloride on jejunal segments in rats. RESULTS: The treated segments without functioning myenteric plexus showed a normal net fluid absorption. Cholera toxin in this segment only induced a reduction of fluid absorption, whereas in a nontreated ileal segment it concomitantly induced a conspicuous net fluid secretion. Intravenous hexamethonium did not change the cholera toxin response in the treated jejunal segments, whereas vasoactive intestinal polypeptide elicited a marked secretion. CONCLUSIONS: Benzalkonium chloride treatment eliminated the ability of cholera toxin to induce intestinal secretion. Thus, all afferent fibers in the intramural secretory reflex activated by cholera toxin are probably conveyed via the myenteric plexus, which functions as the integrating center in the enteric nervous system. The Ussing chamber technique using stripped intestinal preparations cannot be used when studying effects of luminal secretagogues.

Animals↗
PubMed1993

Myenteric plexus destruction alters morphology of rat intestine.

BACKGROUND: It has been shown previously that myenteric plexus destruction by benzalkonium chloride (BAC) increased villus height, crypt depth, and muscle thickness, suggesting that these neurons influence intestinal morphology. A nonspecific trophic effect of BAC, intraluminal stasis, and inflammation resulting from the chemical treatment could also be causes for these changes. Our goals were to (1) show that the morphological sequelae of BAC treatment are caused by myenteric plexus removal and not the factors listed above, and (2) determine whether segmental myenteric plexus removal alters morphology elsewhere in the small intestine. METHODS: Six groups of rats were studied: control, chemical denervation (3 mmol/L BAC), surgical denervation, intraluminal stasis produced by partial obstruction, chemical inflammation (5% acetic acid), and surgical inflammation (serosa removal only). Tissue for histological study was taken from the treated segment, 15-20 cm proximal to the treated segment, and 5-10 cm distal to the treated segment 28 days after treatment. RESULTS: Chemical and surgical denervation reduced the number of myenteric neurons by 94% and 98%, respectively. Denervation had a direct effect on morphology; it increased villus height, crypt depth, and muscle thickness in the treated and proximal segments, but only muscle thickness was increased in the distal segment. The other treatments had minimal morphological sequelae. CONCLUSIONS: Segmental myenteric plexus removal alters the mucosa in the treated and proximal segments but influences muscle thickness throughout the intestine.

Acetates↗
PubMed1995

Electrophysiological and pharmacological responses of chronically denervated lower esophageal sphincter of the opossum.

BACKGROUND & AIMS: Achalasia is characterized by loss of myenteric neurons and incomplete relaxation of the lower esophageal sphincter (LES). The aim of this study was to develop an achalasia model in the opossum using the surfactant benzyldimethyltetradecylammonium chloride (BAC). This study further characterizes the achalasia model. METHODS: BAC or saline was injected circumferentially into the LES of 14 adult opossums. Eight months after injection, manometry, isolated muscle bath studies, electrical field stimulation, and histochemical analysis were performed. RESULTS: Manometrically, the LES of BAC-treated opossums showed higher pressures (38.7 +/- 12 mm Hg vs. 17 +/- 3.0 mm Hg) and reduced esophageal body contraction amplitudes (4.2 +/- 3 mm Hg vs. 27.4 +/- 12 mm Hg). Isolated muscle strips challenged with carbachol and sodium nitroprusside contracted and relaxed similarly to controls. Electrical field stimulation failed to induce relaxation in BAC-treated tissue but did induce contraction. Contractile responses were markedly reduced by tetrodotoxin and atropine in BAC-treated animals and controls. An altered nitric oxide system was shown by the lack of response to L-arginine and N omega-nitro-L-arginine. Histology showed loss of myenteric neurons and increased cholinergic nerve bundles. CONCLUSIONS: Loss of NO inhibitory myenteric neurons markedly reduces the relaxation of the LES, and histology and pharmacological responses suggest a proliferation of cholinergic nerves into the LES contributing to the static elevated pressures of the amyenteric LES.

Analysis of Variance↗